Alzheimer’s disease: can you really catch it?
Evidence emerged today that Alzheimer’s disease might have the potential to spread from one person to the next. Should we be terrified? In short: No.
But the finding could still be game changing because it provides an important clue about how Alzheimer’s and other neurodegenerative diseases like Parkinson’s and motor neurone disease may destroy brain tissue.
Writing today in the journal Nature, a team of scientists from London present evidence that proteins linked to Alzheimer’s – though not the disease itself – may have been passed from person to person. They argue that there is a theoretical risk that such transmission could also happen in the real world through medical procedures.
But their study, limited to just eight people, and proving no link to Alzheimer’s disease itself, is a long way from proving any risk.
According to Prof John Collinge, at University College London, who led the research: “What we’ve found shouldn’t be any cause for alarm. It’s relevant to a very special and rare situation. It’s telling us something about the underlying mechanisms of how these diseases might occur but we’re not saying in any way Alzheimer’s is an infectious disease. You can’t ‘catch’ Alzheimer’s.”
Their conclusions are based on an analysis of a very small, but very unique, group of people. Collinge’s team study the devastating brain-wasting disorder Creuzfeldt-Jakob disease (CJD), which can pass from one person to the next via tissue infected with “prion” proteins.
One group of patients they work with got the disease from human growth hormone injections they received as children between 1959 and 1985. The practice was stopped when it was discovered some batches of hormone – made from the brains of people who donated their bodies for medicine – were contaminated with infectious prions.
A small percentage of patients who received the hormone have gone on to contract, and die, from CJD and their brain tissue has been closely studied by Collinge’s team. While analysing eight recently deceased patients Collinge’s team noticed they had deposits of a protein called amyloid beta in their brain. This is one of the characteristic proteins associated with Alzheimer’s disease.
The patients involved were all far too young to have amyloid protein build-up naturally in their brains – though it is common in elderly brains of people with (and sometimes without) Alzheimer’s. Other patients with CJD who didn’t receive hormone injections had no sign of amyloid. The researchers are concluding that the best explanation for how they got abnormal amyloid in their brain is that it was also transmitted to them via the contaminated hormone injections.
This finding suggests – though it is far from proof – that amyloid could be passed from one person to another. Prion proteins are known to stick very well to stainless steel. As such, an operation using medical instruments on the brain tissue of someone with Alzheimer’s could carry the proteins across to someone without the disease, Collinge warned.
This conclusion is supported by work from Germany which has shown that amyloid protein from mice with a disease similar to Alzheimer’s can be used to “infect” other mice with healthy brains. However, this work only shows the amyloid “pathology” being transferred, not the disease itself. Alzheimer’s disease in humans is characterised by another protein called “tau” – none of which was found in this study. There is still considerable debate as to whether amyloid protein actually “causes” Alzheimer’s or is merely a symptom.
“There is no evidence that Alzheimer’s disease can be transmitted from one person to another, or through use of contaminated surgical instruments, and these results should be interpreted with a great deal of caution,” said Prof David Allsop at the University of Lancaster.
Certainly studies of Alzheimer’s disease in the real world – and there are many – don’t hint at any other causes other than lifestyle factors, genetic risk and age. Studies looking at blood transfusions in people with and without Alzheimer’s, for example, have found no evidence of an effect. Most experts conclude if Alzheimer’s proteins were in some way being transmitted from person to person through some other medical procedure it would likely be at extremely low levels.
But what it does hint at is a possible “paradigm shift,” according to Collinge, in the way a number of degenerative brain diseases work. In recent years there have been a number of experiments showing how Alzheimer’s, Parkinson’s, and forms of motor neurone disease may spread through brain tissue after being “seeded” by a misshapen form of a normal protein. Until recently the only disease known to behave this way was CJD. Prof Collinge is calling for more research to be done on whether contaminated surgical instruments could present a risk.
In a statement the Chief Medical Officer Dame Sally Davies said: “This was a small study on only eight samples. We monitor research closely and there is a large research programme in place to help us understand and respond to the challenges of Alzheimer’s. I can reassure people that the NHS has extremely stringent procedures in place to minimise infection risk from surgical equipment, and patients are very well protected.”
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